Pulmonary Nerves

The lung receives its major sensory and motor innervation from the tenth cranial (vagus) nerve. Pos-taganglionic fibres from the thoracic sympathetic plexus mingle with the vagus fibres as they enter the lung at the hilus. The combined nerves break up into plexuses accompanying the ramifications of the arteries, bronchi, and veins. 

Signal transduction pathway(s) linked to the a-amino - 3 - hydroxy - 5-methyl-4-isoxazolepropionate (AMPA)/kainate receptor subtype plays a major role in transmission of sensory information from the airways to the nucleus tractus solitarii and from nucleus tractus solitarii neurones to the airway vagal preganglionic cells, mediating reflexly increased tracheal blood flow, submucosal gland secretion, and airway tone (Haxhiu et al. 2000). 

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Sulfide can irritate certain pulmonary nerves (e.g., afferent endings of the pulmonary vagi) and high doses can paralyze the ventilatory center. 

One of the primary effects of Mn(II) deficiency is the increased susceptibility to convulsions or seizures which occurs in both ataxic and non-ataxic animals [369]. More recently, there has been increasing evidence that blood levels of Mn(II) are lower in epileptic than in normal patients [370-375]. One hypothesis for the biochemical basis of this effect in the CNS is that lower Mn(II) concentrations in the glial cytoplasm lowers glutamine synthetase activity, which leads to higher extracellular levels of the excitory L-glutamate. This results in a lower firing threshold for neurons with Glu-activated receptors [177]. Other effects of Mn(II) on the nervous system include changes.in the behaviour of cardio-pulmonary nerves [376], effects... 

Pulmonary stretch receptors are responsible for initiating the Hering-Breuer reflex. These stretch receptors are located within the smooth muscle of large and small airways. They are stimulated when the tidal volume exceeds 1 1. Nerve impulses are transmitted by the vagus nerve to the medullary respiratory center and inhibit the inspiratory neurons. The primary function of these receptors and the Hering-Breuer reflex is to prevent overinflation of the lungs. 

However, both sensory and pulmonary irritation can be expected with sufficient exposure. Sensory irritation is characterized by immediate eye and nose irritation that may increase to sensations of burning and pain and is due to interaction between the substance and receptors in the trigeminal nerve. Vapors reaching the lower respiratory tract as well as the lungs may interact with the nerves in these regions, causing dyspnea and breathlessness or pulmonary irritation. 

The aminopyridines (4-aminopyridine 3,4-diaminopyri-dine) accelerate spontaneous exocytosis at central and peripheral synapses. There is also an increase in the number of transmitter quanta released by a nerve action potential. This is probably the result of increased Ca++ inflow at the terminals due to a reduction of K+ conductance and prolongation of the nerve action potential. Muscle strength is increased in patients with the Lambert-Eaton myasthenic syndrome and in others poisoned with botuUnum E toxin (discussed later). Improvement in uncontrolled spasms, muscle tone, and pulmonary function is noted in patients with multiple sclerosis or long-standing spinal cord damage. Side effects that limit clinical utility include convulsions, restlessness, insomnia, and elevated blood pressure. Of the two agents, 3,4-diaminopyridine is the more potent and crosses the blood-brain barrier less readily. 

Primary pulmonary hypertension and cardiac valve disorders have been associated with other centrally acting weight loss agents that cause release of serotonin from nerve terminals although sibutramine has not been associated with these effects in premarketing clinical studies, patients should be informed of the potential for these side effects and monitored closely for their occurrence... 

Despite being a wonder drug against malaria, quinine in therapeutic doses can cause various side-effects, e.g. nausea, vomiting and cinchonism, and in some patients pulmonary oedema. It may also cause paralysis if accidentally injected into a nerve. An overdose of quinine may have fatal consequences. Non-medicinal uses of quinine include its uses as a flavouring agent in tonic water and bitter lemon. 

Increased vascular permeability and oedema Pulmonary artery vasoconstriction Coronary artery vasoconstriction Activation vagal afferent nerves in airways Bronchospasm Gut contraction... 

Serotonin directly causes the contraction of vascular smooth muscle, mainly through 5-HT2 receptors. In humans, serotonin is a powerful vasoconstrictor except in skeletal muscle and heart, where it dilates blood vessels. At least part of this 5-HT-induced vasodilation requires the presence of vascular endothelial cells. When the endothelium is damaged, coronary vessels constrict. As noted previously, serotonin can also elicit reflex bradycardia by activation of 5-HT3 receptors on chemoreceptor nerve endings. A triphasic blood pressure response is often seen following injection of serotonin in experimental animals. Initially, there is a decrease in heart rate, cardiac output, and blood pressure caused by the chemoreceptor response. After this decrease, blood pressure increases as a result of vasoconstriction. The third phase is again a decrease in blood pressure attributed to vasodilation in vessels supplying skeletal muscle. Pulmonary and renal vessels seem especially sensitive to the vasoconstrictor action of serotonin. 

The amphetamines were replaced by amphetamine analogs—substances somewhat less potent than amphetamines. Fen-Phen, the combination of fenfluramine and phentermine, was a popular appetite suppressant in the 1990s, but was associated with severe health problems such as pulmonary hypertension, heart valve dysfunction, and nerve damage. As a result, both drugs were withdrawn from the market. 

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